Neuromuscular Blocking Agents Flashcards
which classes of drugs provide muscle relaxation?
local anaesthetics
benzodiazepines
a2-adrenoreceptor agonists
guaiphenesin
neuromuscular blocking agents
why does ketamine require an adjunct muscle relaxant?
ketamine alone causes muscle rigidity
what is guaiphenesin?
a centrally acting muscle relaxant
where does guaiphenesin act?
internuncial neurones of spinal cord, brainstem and subcortical areas of brain
does guaiphenesin have analgesic/anaesthetic properties?
no
what effect does guaiphenesin have on the blood?
induces haemolysis if given at concentrations over 10%
which concentration of guaiphenesin induces haemolysis?
> 10%
what happens if guaiphenesin is given at concentrations over 10%?
causes haemolysis
how should guaiphenesin be administered?
slow IV only
why should guaiphenesin only be given IV?
causes tissue damage if goes perivascular
when is guaiphenesin typically given?
infused during induction of anaesthesia to reduce rigidity effects of ketamine
can be used in triple anaesthetic protocol in horses
what are the clinical indications for use of NMBAs?
relaxation of skeletal muscles for surgical access
facilitate control of ventilation
facilitate tracheal intubation in cats and pigs
ophthalmic surgery
assist reduction of dislocated joints and fractures
reduction in amount of anaesthetic required
how can NMBAs help with thoracic/abdominal surgery?
can help facilitate retraction in deep abdominal/thoracic surgery
how do NMBAs facilitate control of ventilation?
paralysis of respiratory muscles in order control ventilation more easily
ventilation during thoracotomy
when can NMBAs be useful in reduction of dislocated joints/fractures?
only if injury is recent - less success with longstanding injury
how may use of NMBAs help reduce amount of anaesthetic required?
aids muscles relaxation so that inhalant/injectable can be reduced
what separates the motor neurone and muscle cell?
synaptic cleft
what is separated by the synaptic cleft?
motor neurone and muscle cell
what is released from the nerve endings when a signal is recieved?
acetylcholine
when/where is acetylcholine released?
from the nerve endings when a signal is received
where does acetylcholine bind?
to the post-synaptic nicotinic receptor
how many acetylcholine subunits must be bound to the post-synaptic nicotinic receptor?
two
what does binding of the acetylcholine to the receptors result in?
muscle contraction
how is muscle contraction achieved?
binding of 2 Ach subunits to the post-synaptic nicotinic receptor
what breaks down acetylcholine?
rapidly hydrolysed by acetylcholinesterase within the synaptic cleft
why is muscle contraction short-lived?
ACh is rapidly hydrolysed by acetylcholinesterase
what does acetylcholinesterase do?
hydrolyses acetylcholine
what is very important to remember when considering NMBDs as part of an anaesthetic regimen?
they have no analgesic or anaesthetic effects
what facilities are important to prepare when using NMBDs?
facilities for ET intubation and IPPV
which parts of the body are most and least sensitive to NMBDs?
most effect peripherally and least centrally (diaphragm and intercostals most resistant)
what are depolarising muscle relaxants?
ACh receptor agonists
how do depolarising muscle relaxants work?
They bind to Ach receptors and generate an action potential, but are not metabolised by acetylcholinesterase so they result in extended depolarisation of the muscle end plate (cannot repolarise)
what is the most common depolarising muscle relaxant?
suxamethonium
how is suxamethonium broken down?
by pseudocholinesterase/plasma cholinesterase
what is the onset of suxamethonium?
rapid - 2-3 mins
why is an initial muscle fasciculation seen with depolarising muscle relaxants?
they function by generating a (prolonged) action potential to depolarise the muscle cells
how many doses of suxamethonium can be given?
one
what happens after more than one dose of suxamethonium is given?
phase II block
what is the duration of action of suxamethonium?
3-5 mins in cats
20 mins in dogs
in which species can suxamethonium aid intubation?
cats and pigs
what is usually combined with thiopental during induction of anaesthesia for muscle relaxation in horses?
suxamethonium
what might suxamethonium do to body temperature?
may trigger malignant hypothermia
how does suxamethonium affect serum potassium levels?
increases
why should care be taken using suxamethonium in those with UT issues or CVS instability?
suxamethonium increases serum potassium levels
what is immediate side effect of suxamethonium injection
it burns
what are non-depolarising muscle relaxants also called?
competitive muscle relaxants
how do non-depolarising muscle relaxants work?
they compete with Ach for post-junctional binding sites
why is there no initial muscle fasciculation with non-depolarising muscle relaxants?
they do not generate an action potential
what is the speed of onset of non-depolarising muscle relaxants?
relatively slow
can non-depolarising muscle relaxants be topped up?
yes
how much can non-depolarising muscle relaxants be topped up by?
1/3rd of initial dose
can non-depolarising muscle relaxants be antagonised?
yes
how can non-depolarising muscle relaxants be used for maintained muscle relaxation?
via infusion
what are the 2 most common non-depolarising muscle relaxants?
atracurium and vecuronium
what is atracurium?
a non-depolarising muscle relaxant
what is vecuronium?
a non-depolarising muscle relaxant
how many active isomers are there in atracurium?
1 of a mixture of 10 isomers
what is the active isomer of atracurium called?
cisatracurium
how is atracurium eliminated?
hoffman elimination
what is hoffman elimination?
a temperature-dependent reaction in plasma which eliminates atracurium
what is eliminated by hoffman elimination?
atracurium
why is atracurium the agent of choice for animals with renal/hepatic compromise
undergoes hoffman elimination in plasma rather than breakdown by liver/kidneys
which muscle relaxant is the agent of choice for animals with renal/hepatic compromise?
atracurium
why should atracurium be given slowly IV?
to avoid histamine release
when is laudanosine produced?
can be produced by atracurium metabolism
what can laudanosine produce?
can produce neurological effects - unlikely at clinical doses
where should atracurium be stored?
in the fridge
what is produced by metabolism of atracurium?
laudanosine
what type of molecule is vecuronium?
a steroid compound (no corticosteroid effects)
which non-depolarising muscle relaxant is a steroid compound?
vecuronium
how slowly should vecuronium be administered?
no histamine release - speed of injection less important
how much of a vecuronium dose undergoes hepatic biotransformation?
40-50%
what form does vecuronium come in?
powder which needs reconstituting
how long is vecuronium stable once reconstituted?
24 hours
does vecuronium need to be stored in the fridge?
no
what respiratory parameters are important to monitor when using NMBDs?
ventilation
check tube not kinked/dislodged
ensure breathing system connected
monitor movement of thoracic wall, ETCO2 and SpO2
what are the signs of inadequate depth of anaesthesia while using a NMBD?
increase in pulse rate and blood pressure
salivation/lacrimation
vasovagal response
Increase in ETCO2
slight muscle twitching
pupillary dilation
what can be observed in the vagovagal response?
bradycardia
hypotension
pallor
which nerves can be used with a peripheral nerve stimulator?
ulnar
peroneal
facial
what is the train of 4?
where 4 electrical impulses are applied to the nerve over a 2 second period to assess degree of neuromuscular blockade
can the train of 4 be used to assess anaesthetic depth?
no
which factors affect duration of the neuromuscular blockade?
dose administered
volatile agent
hypothermia (prolongs)
hepatic/renal insufficiency (prolongs)
electrolyte and acid-base abnormalities
muscle diseases (e.g. myasthenia gravis)
aminoglycoside abs (prolongs)
what effect do muscle diseases (e.g. myasthenia gravis) have on neuromuscular blocking?
they greatly potentiate effect of the NMB agent - care with dose!
how long do normal clinical doses of NMBDs last?
20-30 mins
what are the main anticholinesterases called?
neostigmine and edrophonium
what does acetylcholinesterase do?
breaks down acetylcholine
what do anticholinesterases do?
interfere with the action of acetylcholinesterases
how do anticholinesterases antagonise non-depolarising NMBs?
interfere with action of acetylcholinesterases - less is broken down so Ach concentration increases and competes with NMB agent for post-synaptic receptor
what unwanted side-effects may be seen with use of antocholinesterases?
bradycardia
salivation
bronchospasm
diarrhoea
which anticholinergic drugs are administered with anticholinesterase?
atropine or glycopyrrolate
when can supported ventilation be ceased when using NMBDs?
when spontaneous ventilation returns
what should be closely monitored on recovery when patients have had a NMBD?
URT weakness on recovery - swallowing reflex but then return of paralysis
URT sounds
cyanosis
paradoxical ventilation
inadequate respiratory effort
why are anticholinergic agents given if antagonising non-depolarising muscle relaxants?
to lessen bradycardic effects
